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Can PPAR Keep Cadmium in Check?PPAR 能控制镉吗?
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Cadmium-mediated lung injury is exacerbated by the persistence of classically activated macrophages.镉介导的肺损伤会被经典激活型巨噬细胞的持续存在所加剧。
J Biol Chem. 2020 Nov 13;295(46):15754-15766. doi: 10.1074/jbc.RA120.013632. Epub 2020 Sep 11.
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J Hazard Mater. 2018 Sep 5;357:355-362. doi: 10.1016/j.jhazmat.2018.06.003. Epub 2018 Jun 1.
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本文引用的文献

1
A new insight into the treatment of diabetes by means of pan PPAR agonists.通过泛PPAR激动剂治疗糖尿病的新见解。
Chem Biol Drug Des. 2022 Dec;100(6):947-967. doi: 10.1111/cbdd.14020. Epub 2022 Jan 17.
2
Receptor-Interacting Protein Kinase 3 Inhibition Prevents Cadmium-Mediated Macrophage Polarization and Subsequent Atherosclerosis Maintaining Mitochondrial Homeostasis.受体相互作用蛋白激酶3抑制可预防镉介导的巨噬细胞极化及随后的动脉粥样硬化 维持线粒体稳态
Front Cardiovasc Med. 2021 Nov 8;8:737652. doi: 10.3389/fcvm.2021.737652. eCollection 2021.
3
Subacute cadmium exposure promotes M1 macrophage polarization through oxidative stress-evoked inflammatory response and induces porcine adrenal fibrosis.亚急性镉暴露通过氧化应激诱发的炎症反应促进M1巨噬细胞极化并诱导猪肾上腺纤维化。
Toxicology. 2021 Sep;461:152899. doi: 10.1016/j.tox.2021.152899. Epub 2021 Aug 18.
4
Cigarette smoke exposure and alveolar macrophages: mechanisms for lung disease.香烟烟雾暴露与肺泡巨噬细胞:肺部疾病的发病机制。
Thorax. 2022 Jan;77(1):94-101. doi: 10.1136/thoraxjnl-2020-216296. Epub 2021 May 13.
5
PPAR Gamma: From Definition to Molecular Targets and Therapy of Lung Diseases.过氧化物酶体增殖物激活受体γ:从定义到肺部疾病的分子靶点和治疗。
Int J Mol Sci. 2021 Jan 15;22(2):805. doi: 10.3390/ijms22020805.
6
The adverse impact of cadmium on immune function and lung host defense.镉对免疫功能和肺部宿主防御的不良影响。
Semin Cell Dev Biol. 2021 Jul;115:70-76. doi: 10.1016/j.semcdb.2020.10.007. Epub 2020 Nov 3.
7
Cadmium-mediated lung injury is exacerbated by the persistence of classically activated macrophages.镉介导的肺损伤会被经典激活型巨噬细胞的持续存在所加剧。
J Biol Chem. 2020 Nov 13;295(46):15754-15766. doi: 10.1074/jbc.RA120.013632. Epub 2020 Sep 11.
8
Maresin1 Promotes M2 Macrophage Polarization Through Peroxisome Proliferator-Activated Receptor-γ Activation to Expedite Resolution of Acute Lung Injury.maresin1 通过激活过氧化物酶体增殖物激活受体-γ促进 M2 型巨噬细胞极化,从而加速急性肺损伤的修复。
J Surg Res. 2020 Dec;256:584-594. doi: 10.1016/j.jss.2020.06.062. Epub 2020 Aug 14.
9
Macrophage polarization and its role in the pathogenesis of acute lung injury/acute respiratory distress syndrome.巨噬细胞极化及其在急性肺损伤/急性呼吸窘迫综合征发病机制中的作用。
Inflamm Res. 2020 Sep;69(9):883-895. doi: 10.1007/s00011-020-01378-2. Epub 2020 Jul 10.
10
Low-dose cadmium potentiates lung inflammatory response to 2009 pandemic H1N1 influenza virus in mice.低剂量镉增强了 2009 年大流行 H1N1 流感病毒在小鼠肺部的炎症反应。
Environ Int. 2019 Jun;127:720-729. doi: 10.1016/j.envint.2019.03.054. Epub 2019 Apr 15.

PPAR 能控制镉吗?

Can PPAR Keep Cadmium in Check?

机构信息

Department of Internal Medicine, Division of Allergy and Immunology, Morsani College of Medicine, University of South Florida, Tampa, FL 33612, USA.

出版信息

Biomolecules. 2022 Aug 9;12(8):1094. doi: 10.3390/biom12081094.

DOI:10.3390/biom12081094
PMID:36008989
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9405879/
Abstract

Cd, a naturally occurring endocrine toxin found in tobacco leaves, originates in the environment and enters the body through inhalation, targeting the lungs and kidneys. A study published by Larsen-Carey et al. revealed that cadmium mediates the persistence of classically activated lung macrophages to exacerbate lung injury. The research discovered a novel role for PPAR as an effective regulator for the alternative activation of macrophages in response to Cd and Cd-induced lung injury.

摘要

镉(Cd)是一种存在于烟草叶中的天然内分泌毒素,来源于环境,通过吸入进入人体,主要侵害肺和肾。拉森-凯里等人发表的一项研究表明,镉介导经典激活的肺巨噬细胞持续存在,从而加重肺损伤。该研究发现了 PPAR 的一个新作用,即作为一种有效调节剂,调节巨噬细胞对 Cd 及 Cd 诱导的肺损伤的另一种激活方式。